To replicate and cause disease, HIV-1 must overcome cellular and humoral immune responses, defeat innate cellular defense systems, usurp cellular factors, and reprogram the normal biology of the cell. Historically, detailed genetic analyses of viral functions and evolution have identified key viral determinants for the successful completion of each stage in the replication cycle. More recently, studies of innate antiviral and immune responses, host genetics, cell biology, and neuropathogenesis have identified host factors that HIV-1 must overcome in order to replicate. The field is now poised to combine these studies to define the molecular mechanisms that underlie important host/virus interactions, and our meeting, therefore, focuses on emerging concepts in the molecular mechanisms of HIV pathogenesis. By bringing together a group of international leaders in HIV/AIDS research, new and exciting information in all of these areas will be presented, new paradigms will be established, and, perhaps, new approaches for anti-HIV therapeutics will be identified. Given the "style" of Keystone Symposia, the ample time for discussion will facilitate collaborative efforts that will exploit the diverse areas of expertise of the attendees. Also, and of particular importance, our proposed speaker program includes a mixture of senior and less-senior investigators. We expect that this will enhance the attractiveness and success of the Symposium by providing exposure to a broad range of research groups and their areas of interest. Finally, many of the oral sessions include places for "abstract-driven" presentations. This is intended to increase the number and quality of submitted abstracts and to stimulate greater participation of non-invited scientists; this will also ensure that the very latest developments in the field of HIV Pathogenesis will be presented and discussed.